New research reveals potential treatment to delay and manage osteoarthritis (IMAGE)
Caption
Primary chondrocytes overexpressing HDAC6 genetically were generated via plasmid transfection. The up-regulation of HDAC6 can deacetylate tubulin in the microtubule system, which interferes with spatial arrangement of mitochondria, leading to degradation of the extracellular matrix (ECM) and up-regulation of reactive oxygen species (ROS). Inhibition of enzyme activity of HDAC6 by Tubastatin A reverses these results and postpones the development of osteoarthritis.
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The American Journal of Pathology
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